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pubmed:abstractText |
Human low density lipoproteins are metabolized by cultured human fibroblasts, through a specific metabolic pathway, which entails the regulation of intracellular cholesterol synthesis. When anti-lipoprotein IgA coming from patients with myeloma, mixed hyperlipidaemia and xanthomatosis were introduced into the system, we observed a decrease of the protein degradation of the LDL molecule, and a disappearance of the regulation of intracellular cholesterol synthesis. In the same system, an anti-lipoprotein IgA from a case of myeloma with mixed hyperlipidaemia, but without xanthomatosis, or control IgG and IgA were inactive and did not modify the LDL pathway.
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